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104
3 Neurosonography in Neonates, Infants and Children
Infarction in older child :
US not routinely used for diagnosis, but helpful for bedside follow-up (vessel
patency, perfusion state during neuro-resuscitation therapy, etc.). Usually no gray
scale fi ndings, just (a)CDS helpful.
Specifi c use of transcranial CDS: assessment of infarction risk by monitoring
children with sickle cell disease (see below).
3.3.5.4 (C)DS in Brain Hypoxia
General remarks : for spectral fl ow analysis, always consider potential infl uence of
other systemic factors such as ventilation, medication, cardiac output, heart rate, etc.
Focal ischemia – aCDS may depict lack of fl ow signals in affected area:
• With some delay – reactive perifocal hyperaemia (“luxury perfusion”).
• If main vessels and large area affected – asymmetric fl ow profi les on spectral
analysis of corresponding feeding arteries.
Global/general hypoxia and brain oedema – typical phases (Fig. 3.26 ):
• Phase I : normal vascular anatomy with normal fl ow spectra (up to 24 h after event).
• Phase II – reperfusion and hyperaemic phase : increasing diastolic fl ow, poten-
tially also increased systolic velocity and decreased resistive index – these fi ndings usually associated with risk of only mild neurologic defi cit.
• Phase III – increasing brain pressure : if process cannot be controlled in stage II,
increasing oedema causes increasing peripheral resistance and rising intracranial
pressure. Initially leads to reduction of diastolic, then also systolic fl ow velocities. Consecutively and constantly increasing RI values. In transition phase RI
values may become (pseudo-)normal, before they progress. If typical phase III
pattern with reduced systolic velocity and elevated RI due to signifi cantly
reduced diastolic fl ow depicted – high probability of severe neurologic defi cits
with worst prognosis in those infants where these fi ndings persist longer.
Fig. 3.26 Flow spectra in brain oedema –
various stages. ( a ) Initial stage – normal fl ow.
( b ) Hyperaemic phase, high diastolic fl ow.
( c ) Beginning intracranial pressure, tent-shaped
diastolic fl ow. ( d ) Increasing intracranial pressure,
reversed diastolic fl ow. ( e ) Short spikes without
antegrade perfusion in brain death
a
b
c
d
e
3.3 Pathologic Findings
105
• Another typical pattern of phase III: tent-shaped diastolic fl ow spectrum with
lower end systolic and early diastolic velocity, higher velocity in mid-diastole
and again low end-diastolic velocity.
• Phase IV : with increasing pressure fl ow becomes increasingly pulsatile with
reversed diastolic fl ow, increasingly reduced systolic fl ow velocities, eventually
only showing undulating signals with no suffi cient antegrade perfusion – as all
blood infl ow during systole fl ows out during diastole – constitutes lack of brain
perfusion and inevitably leads to brain death.
• Phase V – brain death : lack of parenchymal perfusion and no fl ow seen in major
vessels.
• These phenomena apply also to older children in ICU for bedside monitoring.
NOTE : Confi rm severe fi ndings by (C)DS of cervical vessels and/or by ce-US; in
some countries persisting fi ndings of phase IV (+ eventually phase V) accepted for
diagnosing brain death (repeated examinations mandatory). Missing or reversed
diastolic fl ow with low systolic fl ow velocities or tent-shaped diastole indicate poor
prognosis.
Other applications of (C)DS:
• (C)DS can be utilised to titrate optimal PCO
for ventilation support at the bed-
2
side by performing duplex studies while altering respirator settings under constant PCO 2 monitoring, thus defi ning PCO 2 level which correlates with most
normal fl ow profi les – to avoid perfusion defi cits and hyperperfusion (which
increases brain oedema risks).
• TCI-DS for monitoring sickle cell anaemia : screening for overt or silent infarc-
tion and risk of (re-)infarction – high fl ow velocities = reliable predictor of
stroke. Time-averaged mean of maximum or maximum systolic velocity
velocities (TAMx) of MCA most commonly used and performed in children:
normal <170 cm/s, conditional = 170–200 cm/s, abnormal >200 cm/s.
Standardised assessment of all major vessels essential, potentially include cervical arteries.
3.3.6 Inflammation
Introduction
US only shows indirect changes (signs that may be compatible with infl ammation)
or complication (e.g. abscess formation and haemorrhage). Final diagnosis always
needs other tests (lumbar puncture, blood samples, MRI, etc.).
MRI method of choice for evaluating central nervous system complications –
particularly in older children.
NOTE : In spite of existing infection, US fi ndings may be completely normal.
3.3.6.1 Prenatal Intrauterine Infections and Residuals
Common causes for prenatal CNS infections are cytomegalovirus, herpes, toxoplasma, HIV and rubella (TORCH). Less common than in earlier times, but still
exist and lead to various postnatal US fi ndings.
106
3 Neurosonography in Neonates, Infants and Children
ab
Fig. 3.27 Intracranial/cerebral calcifi cations. ( a ) Frontal coronal view: spotted multifocal cerebral
calcifi cations in the white matter after fetal TORCH infection. ( b ) Parasagittal view: non- calcifying
vasculopathy ( arrows )
Postnatal US Findings :
• Hydro-, micro- and macrocephalus.
• Intracerebral calcifi cations, band-like or stippled – most commonly in area of
basal ganglia (small echogenic foci, commonly without acoustic shadowing)
(Fig.
3.27a ).
• Non-calcifying vasculopathy as remnant of vascular involvement: band-like
echogenic stripes, particularly in basal ganglia along perforating arteries (not specifi c, many other entities that affect vessels and perivascular bed) (Fig.
3.27b ) –
see also entry 3.9 .
• Hemispheric calcifi cation occur, can be large – see also 3.3.9
• Porencephalic defects, multicystic encephalopathy and atrophy.
• Differentiation of metabolic causes, remnants of other prenatal CNS complications, remnants of prenatal haemorrhages, ischemic changes, etc. from (TORCH)
infections may be diffi cult.
3.3.6.2 Postnatal Inflammation
Meningitis
• Bacterial meningitis: widening of extra-axial CSF spaces with internal echoes,
may have debris/CSF layering (Fig. 3.28a , Brain).
• Some correlation of distribution of fi ndings with aetiology, e.g. tuberculous meningitis often manifests basally.
• Empyema may occur (Fig. 3.28b ).
NOTE : Postinfl ammatory hydrocephalus may develop – children should have fol-
low-up imaging.
Meningoencephalitis
• Commonly viral – fi ndings subtle.
• If brain involved: focally altered echogenicity similar to fi ndings in infarction or
ischemia.
• Secondary haemorrhage may occur, particularly in herpes encephalitis.
3.3 Pathologic Findings
107
a
Fig. 3.28 Brain US in infl ammatory conditions. ( a ) Coronal view, near fi eld, linear transducer:
purulent meningitis – echogenic content in extra-axial CSF space, echogenic and thick arachnoid.
( b ) Coronal view, sector transducer: frontoparietal empyema (+ +). ( c ) Coronal view: subcortical
brain abscess (+ +)
b
c
• Sequelae cannot be distinguished from other causes. Manifest as focal atrophy,
porencephalic and cystic defects, hydrocephalus and calcifi cations.
• If calcifi cation-like echoes seen in early stages of disease, consider rare or atypical aetiology (e.g. fungal infection and echinococcal abscess).
Ventriculitis and Brain Abscess
• Typical fi nding: thickened echogenic ependyma of ventricular wall with irregularly thickened swollen choroid plexus.
• CSF in ventricles shows echoes and sedimentation, which vary with brain
positioning.
• Complications: hydrocephalus, compartmentisation of ventricular lumen and
isolated (fourth) ventricle (see hydrocephalus 3.3.6).
• Brain abscess: focal echogenicities with relatively sharp borders, surrounded by
hypoechoic oedematous rim and eventually central inhomogenously hypoechoic
space (central necrosis). With ongoing disease central necrosis becomes larger,
wall-like demarcation of abscess, eventually with thick capsule (Fig. 3.28c, d ).
• Haemorrhages or vascular malformations may initially be diffi cult to differentiate from abscess by US. Only by monitoring the imaging course of disease (with
better differentiation of necrosis and detritus as well as sedimentation) and with
clinical information the aetiology becomes evident.
NOTE : Abscesses may connect with ventricular lumen.
CDS in Mening(oencephal)itis
May demonstrate hypervascularity of meninges as well as around capsule of abscess.
• Flow spectrum exhibits diastolic hyperaemia with elevated diastolic fl ow velocity and low RI values (additional diagnostic hint).
3.3.7 Dilatation of CSF Spaces: Hydrocephalus
Introduction and Defi nition
Hydrocephalus – dilatation of internal and/or external CSF spaces. Dilatation does
not mean increased intracranial pressure – there can be dilatation without increased
pressure and also increased pressure without dilatation.
108
3 Neurosonography in Neonates, Infants and Children
a
b
c
Fig. 3.29 US in dilated extra-axial CSF space. ( a ) Linear transducer, coronal view: benign sub-
dural effusion/familial macrocephaly (DDx atrophy). ( b ) Coronal view: SDH after overshunting in
hydrocephalus. ( c ) Axial view by TCI: chronic, septated temporo-occipital SDH
NOTE : Only increased intracranial pressure needs treatment.
Task of US :
• Depiction of dilatation/widened ventricles or external CSF spaces.
• Potentially recognise cause of dilatation.
• Find signs that indicate elevated intracranial pressure.
The Most Common Causes :
• Posthaemorrhagic or postinfl ammatory.
• Associated with malformations.
• Secondary to obstruction of CSF drainage:
– Dysfunction of ventriculoperitoneal shunt, outfl ow path stenosis, or space
occupying lesion, adhesions, etc.
• Ex-vacuo – atrophy:
– For example, after severe hypoxia, metabolic disease and postinfection.
• Normal variants (i.e. macrocephaly, ventriculomegaly and benign familiar external hydrocephalus/“frontal effusion”/familial benign macrocrania) (Fig.
3.29a ).
• After trauma (e.g. shaken baby syndrome).
• Increased CSF production (hypersecretory hydrocephalus):
– For example, after infl ammation or haemorrhage and choroid plexus
papilloma.
• Reduced resorbtion of CSF:
– For example, increased central venous pressure, venous sinus thrombosis,
third space phenomena, jugular vein obstruction and arachnoid granulation
dysfunction.
3.3 Pathologic Findings
109
US Appearance
Dilatation of CSF spaces which usually appear anechoic.
Extracerebral CSF spaces:
• Through fontanel – best seen with high-resolution linear transducers in coronal
section (widening of interhemispheric fi ssure) or when using sector array in
slightly angled coronal section (Fig. 3.29a, b ).
• Transtemporal/mastoid approach – allows visualisation of contralateral external
extra-axial CSF spaces – also useful for arachnoid cysts, CSF spaces of posterior
fossa and posterior horn of lateral ventricles (Fig. 3.29c ).
US fi ndings in dilated ventricles
Confi guration of ventricles helps differentiating supra- from infratentorial or global
hydrocephalus:
• Foramen of Monro occlusion – dilated repective affected lateral ventricle with
small third and fourth ventricle.
• Aqueductal stenosis – lateral ventricles and third ventricle dilated (supratentorial
hydrocephalus) (Fig. 3.30a–c ).
• Obstructed foramina of Luschka and Magendie – all ventricles dilated, usually
combined with narrow extra-axial CSF spaces.
• Additional obstruction in subarachnoid space – dilated cisterns.
• Obstruction above and below fourth ventricle – isolated fourth ventricle
(Fig. 3.30d ) – only fourth ventricle dilated, particularly if supratentorial ven-
tricular system shunted and drained (rare condition, e.g. after infection, surgery
or haemorrhage).
Other US criteria – signs that may allow differentiating aetiology:
• Echogenic content – haemorrhage or severe infection.
• Echogenic thickened ventricular wall – ependymitis (nonbacterial infl ammatory
reaction after haemorrhage due to resorptive phenomena, after ventriculitis, etc.),
with chronically increased pressure.
• Calcifi cations – after infection and ischemia, particularly in basal ganglia.
• Residual choroid plexus or parenchymal lesions – posthaemorrhagic, postischemic, posttraumatic, etc.
Signs for increased intraventricular and/or intracranial pressure :
• Inhomogenous structure around ventricles, potentially some small hyperechoic
cystic lesions – sign for either focal hypoxia or posthaemorrhagic or venous
infarction (e.g. due to obstruction of draining periventricular veins during ventricular dilatation).
• Ballooning of temporal horn.
• Narrowing of external CSF spaces.
• Ventricles can be very narrow or slit like (e.g. in brain oedema after hypoxia).
• Extra-axial cause for increased brain pressure due to focal pathology (arachnoid
cyst, subdural/epidural haemorrhage/effusion) – locally compressed parenchyma, fl attened brain surface and potentially midline shift.
Differentiation epidural/subdural from subarachnoid space :
• Subarachnoid space – reaches into sulci, has network of crossing vessels and
mildly echoic lines.
• Subdural space – does not reach into sulci, usually anechoic and only a few
major bridging veins ⇨ use aCDS.
110
3 Neurosonography in Neonates, Infants and Children
a
b
cd
e
Fig. 3.30 Hydrocephalus. ( a ) Coronal view: supratentorial hydrocephalus, dilated lateral ventri-
cles (+ +
occluded. ( c ) Stenosed, but still patent aqueduct – fourth ventricle nicely fi lled. ( d ) Open aqueduct
with huge dilatation of forth ventricle on axial view by TCI. ( e ) Coronal view: dilated “isolated”
fourth ventricle (the supratentorial ventricular system is drained – otherwise one will have to consider severe hypoplasia of the cerebellum)
1,2
) and third ventricle. ( b ) TCI: Supratentorial hydrocephalus – aqueduct appears
NOTE : In chronic and recurrent subdural effusion, multiple septae and layers of
different echogenicity may occur.
Role of CDS in Increased Intracranial Pressure
Early phase, only slight increase in intracranial pressure – normal or slightly reduced
resistive index (RI) (reactive diastolic hyperaemia), generally increased fl ow
velocities.
3.3 Pathologic Findings
111
a
Fig. 3.31 Doppler in hydrocephalus. ( a ) Slightly elevated brain pressure, indicated by change of
fl ow profi le in intra-/extracranial ICA portion measured from fontanellar access in a coronal section. ( b ) TCI-Doppler for measuring fl ow response during fontanellar pressure (“ druck ”): no sig-
nifi cant change in MCA fl ow pattern in this preterm baby with posthaemorrhagic hydrocephalus
b
When pressure gets higher:
1. Diastolic fl ow velocity decreasing – elevated RI:
• There may be tent-shaped antegrade diastoly in early phases – similar to
severe hypoxia.
2. Systolic velocities decreasing – transient “pseudo-normal” RI.
3. Diastole more affected ⇨ reversed diastolic fl ow, RI > 100 %:
• Sometimes diffi cult to differentiate from other systemic reasons such as PDA.
• Severely increased brain pressure – eventually leads to signifi cant reduction
of systolic fl ow velocity and signifi cant arterial perfusion defi cit (see also:
brain oedema and brain death).
Other techniques to depict increased brain pressure
Fontanellar pressure : apply gentle pressure on fontanel with fi nger while per-
forming DS of one of major basal vessels (commonly MCA) – in case of signifi cantly increased brain pressure fi rst diastolic and then systolic fl ow velocities
reduced during manoeuvre (Fig. 3.9 ).
DS of ICA at extra- and intracranial portion from transfontanellar access
( Fig. 3.31 ) : fontanellar DS visualises ICA siphon coursing into head (both in coronal and parasagittal view) – place duplex gate for spectral trace in extracranial and
intracranial ICA portion (Fig.
and extracranial velocities and RIs ( equation = V
V
extracranially):
syst max
3.31 , Brain), calculate ratio between systolic intra-
intracranially divided by
syst max
• Normal – fl ow spectra do not differ, velocity ratio = 1 (0.8–1.2).
• Slightly increased brain pressure (<10 mmHg) – slight elevation of systolic fl ow
velocity intracranially and only mild variation of diastolic fl ow, velocity
ratio = >1.2.
• Signifi cantly elevated brain pressure (>10 mmHg) = altered systolic + diastolic
fl ow, velocity ratio <0.8.
112
3 Neurosonography in Neonates, Infants and Children
a
Fig. 3.32 US/TCI in shunted hydrocephalus – mostly used in slightly older infants with (nearly)
closed fontanel. ( a ) TCI: two drains, one in each lateral ventricle, with different ventricular disten-
sion. Note a slight subdural effusion on the side with the smaller ventricle as a sign of overshunting. ( b ) TCI, axial view, 9 month old infant: shunted hydrocephalus (shunt = arrow ), still
large ventricles
b
ab
Fig. 3.33 US for assessing complications in shunted hydrocephalus. ( a ) Linear transducer, neck:
disruption (+ +) of subcutaneous portion of shunt. ( b ) Fluid pouch in superfi cial subcutaneous soft
tissue next to the drain ( arrow ) that is disconnected
US for following up hydrocephalus with/without shunts :
• All basic US criteria apply.
• Additionally try to visualise shunt drain: course, tip of drain and look for drain
discontinuity.
NOTE : Can be diffi cult, often transtemporal or transmastoid access necessary
(Fig. 3.32 ). Tip of shunt may be less echogenic than more peripheral part and
missed, depending on US beam angle and access:
• Always assess valve (effusion?).
• Try to follow extracranial partition of drain (subcutaneous track in skull, neck
and chest easily seen) – disruption – focal fl uid effusions along drain path due to
leakage/rupture (Figs. 3.32b and 3.33 ).
• CDS: achievable if cellular components in CSF (if sound can penetrate –
depending on material of shunt).
• Assess abdominal part of shunt: pseudocyst around intraabdominal tip may
cause obstruction, free peritoneal/pleural fl uid help to indicate drain function,
evaluate for peritonitis in children with pain, etc. (Fig. 8.26 ).
3.3 Pathologic Findings
113
a
b
c
Fig. 3.34 Special applications of modern US in hydrocephalus. ( a ) Magnifi ed fontanellar sagittal
midline view: CDS demonstrates CSF fl ow in aqueduct. ( b ) Duplex Doppler trace confi rms bidi-
rectional undulating CSF fl ow. ( c ) 3DUS in hydrocephalus: three orthogonal views and rendered
lateral ventricles
NOTE : US may fi nd causes of obstruction or dysfunction and can depict size
increase of CSF space or perfusion deterioration due to increased brain pressure.
However, US does not depict/rule out all causes of potential shunt complications,
chronically or moderately increased brain pressure, stiff ventricle syndrome, etc.:
• CDS may show CSF fl ow in foramina of Monro, Magendie and Luschka and
aqueduct – provided that there are refl ectors in CSF (e.g. posthaemorrhagic particles, increased CSF protein levels and infl ammatory cells) (Fig. 3.34a, b ).
• Unusual access to extracerebral CSF spaces – use eye/orbit as US window. In
increased intracranial pressure – optic nerve sheet dilatation and protrusion of
papilla (see: US of eye).
• In CSF fi stula: US may demonstrate fi stula (if large enough and accessible) and
show fl ow through fi stula by aCDS if particles in CSF or relatively high fl ow